The Undiscovered Country

Needs a Ring Job, New Clutch

But for now let's leave aside the question of how long humans can live and concentrate instead on why most of us will not live to see the century mark. In 1990, the illustrious Russian biologist Zhores Medvedev sought to classify the more than 300 theories that had been put forth to account for this ineluctable reality. Many of these theories, compelling in their own right, likely capture some of the underpinnings of our mortality. Their sheer number, however, suggests as much about the complexity of the question as it does about the difficulty of thinking dispassionately about death. Scientists, after all, are people who are going to die too.

Theories of death are also deeply embedded in their culture of origin. Let's consider, for instance, the class of mechanical explanations of death. These hypotheses invite us to accept the metaphor of the human body as a machine with many parts that must work in concert. In this metaphor, we die either because a key component gives way (the catastrophic failure model) or because several interacting parts begin to wear out and no longer work properly (the systems failure model). These metaphors of failing machinery compel, but data supporting them are harder to obtain. Catastrophic failures, like heart attack and stroke, are major killers in the developed world, particularly in the United States. Many of these deaths, however, are preventable and linked to a sedentary lifestyle, and not to an inherent age-dependent failure of a particular organ system.

The systems-based explanation argues that complex machinery fails because many things go wrong. According to this model, as with your Toyota, so too with your body: The force-of-mortality curves for automobiles (called failure-rate curves) complied by demographers James W. Vaupel and Cynthia R. Owens at Duke University bear an uncanny resemblance to their human counterparts. Both human and automobile curves show an exponential increase in the force of mortality that tapers off in later years—the same violation of the Gompertz Law we spoke of earlier. Surprisingly, mortality in the early years is eerily similar in people and automobiles: Defects in manufacture (machines) or development (organisms) reveal themselves early on. But if you (or your car) make it past the first year, you're likely to motor along for a good period thereafter. The patterns are tantalizing in their similarity and may reveal some fundamental features of failure in complex systems. Such systems, whether we speak of Toyotas or biologists, are characterized by redundancy brought about by engineering (in the first case) or evolution (in the second). But, as University of Chicago gerontologists Leonid Gavrilov and Natalia Gavrilova have argued in their influential bookThe Biology of Life Span: A Quantitative Approach, the very redundancy that permits complex systems to endure a constant rain of light damage also allows such damage to accumulate, resulting in aging and eventual failure. Surprisingly, the higher the level of redundancy, the faster the force of mortality accelerates with age. The irony is that the redundant mechanisms that ensure survival during our early years are the same ones that speed our twilight exit.

For two centuries, biology has profited from Rene Descartes's conception of the human body as a machine, subject to, and more importantly, explainable by, material laws. Compelling as the Cartesian metaphor of the body-as-machine might be, it may, however, conceal some important differences between my automobile and me. Repair, for instance, is a process central to survival. I depend on my excellent mechanic, an agent external to my automobile, to keep my car on the road. In contrast, bodies, for the most part, repair themselves: More than 100 genes in our genome are devoted to detecting and repairing DNA damage.

This notion of the body as a self-policing, self-correcting system has spawned a second class of death explanations, those related to maintenance. Although the human body can detect and remedy a startling array of defects, this capacity to self-renew declines with age. Even the raw materials for repair—those stem cells recruited to replace exhausted counterparts—become depleted. The damage to our bodies, meanwhile, continues unabated throughout our lives. Much like the inventive mechanics in Cuba who keep Edsels and Cadillacs from the '50s running without spare parts, the body struggles to patch up broken functions as replacement cells decline. But it is, ultimately, a losing battle. In a final ironic twist, the repair process, like the existence of redundancies, becomes a source of trouble as we get older. The inflammation that accompanies injury and repair is itself a source of further damage. Aging and death may come about when we can no longer keep up with the maintenance required to stay alive.